Plasma membrane-derived vesicles (PMVs) are released into circulation in response to normal and stress/pathogenic conditions. They are of tremendous significance for the prediction, diagnosis, and observation of the therapeutic success of many diseases. Knowledge of their functional properties would contribute to a better understanding of the pathological mechanisms leading to various diseases in which their levels are raised. The objective of this study was to quantify and compare the levels of PMVs in sickle cell disease patients (Hb SS and Hb SC) with non-sickle cell (Hb AA) subjects. The comparison will help us research and understand the processes that lead to their constitutive release in sickle cell disease patients than in their normal counterparts. A total of one hundred and fifty (150) sickle cell disease patients (study group) and blood donors (control group) that consented to partake in the study were recruited. There were 82 males and 68 females. Fifty (50) each of Hb SS, Hb SC and Hb AA samples were obtained. Sodium metabisulphite (sickling) test, Haemoglobin electrophoresis and quantification of PMVs were carried out on all the samples. The sickle cell disease patients had elevated levels; SS (38.89 ± 0.73 × 104/ml; p= 0.01) and SC (32.62 ± 1.18 × 104/ml; p = 0.01) as against the control subjects (Hb AA) who had average PMVs of 11.28 ± 0.29 × 104/ml PFP (mean ± SEM). It was concluded that both SS and SC (study) samples showed an increased count of PMVs as compared to the AA (control) samples, suggesting persistent endothelial stimulation and/or injury of blood cells leading to continuous shedding of PMVs in sickle cell disease patients.
Published in | American Journal of Biomedical and Life Sciences (Volume 1, Issue 4) |
DOI | 10.11648/j.ajbls.20130104.14 |
Page(s) | 99-102 |
Creative Commons |
This is an Open Access article, distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution and reproduction in any medium or format, provided the original work is properly cited. |
Copyright |
Copyright © The Author(s), 2013. Published by Science Publishing Group |
PMVs, Sickle Cell Disease, Electrophoresis, Flow Cytometer
[1] | Perumbeti A, Malik P (2010). Genetic correction of sickle cell anemia and β-thalassemia: progress and new perspective. The Scientific World Journal 10: 644–654. |
[2] | Kato GJ, Hebbel RP, Steinberg MH, Gladwin MT (2009). Vasculopathy in sickle cell disease: Biology, pathophysiology, genetics, translational medicine, and new research directions. Am J Haematol 84(9): 618-625. |
[3] | Lionnet F, Hammoudi N, KS Stojanovic1, AvellinoV, Grateau G, Girot R and Haymann JP (2012). Hemoglobin SC disease complications: a clinical study of 179 cases. Haematol 97(8): 1136-1141. |
[4] | Ballas SK, Lieff S, Benjamin LJ, Dampier CD, Heeney MM, Hoppe C, Johnson CS, Rogers ZR, Smith-Whitley K, Wang WC, Telen MJ (2010). Definitions of the phenotypic manifestations of sickle cell disease. Am J Haematol 85(1): 6-13. |
[5] | Morel O, Hugel B, Jesel L, Zobairi F, Bareiss P, Freyssinet JM, Toti F (2004). Procoagulant membranous microparticles and atherothrombotic complications in diabetics. Arch Mal Coeur Vaiss 97(10): 1006-1012. |
[6] | Boulanger CM, Scoazec A, Ebrahimian T, Henry P, Mathieu E, Tedgui A, Mallat Z (2001). Circulating microparticles from patients with myocardial infarction cause endothelial dysfunction. Circulation 104(22): 2649-52. |
[7] | Baj-Krzyworzeka M, Majka M, Pratico D, Ratajczak J, Vilaire G, Kijowski J, Reca R, Janowska-Wieczorek A, Ratajczak MZ (2002). Platelet-derived microparticles stimulate proliferation, survival, adhesion, and chemotaxis of hematopoietic cells. Exp Hematol 30(5): 450-459. |
[8] | Freyssinet JM, Toti F, Hugel B, Gidon-Jeangirard C, Kunzelmann C, Martínez MC, Meyer D (1999). Apoptosis in vascular disease. Thromb Haemost 82(2): 727-735. |
[9] | Tan KT, Tayebjee MH, Lynd C, Blann AD, Lip GY (2005).Platelet microparticles and soluble P selectin in peripheral artery disease: relationship to extent of disease and platelet activation markers. Ann Med 37(1): 61-66. |
[10] | Shet AS, Aras O, Gupta K, Hass MJ, Rausch DJ, Saba N, Koopmeiners L, Key NS, Hebbel RP (2003). Sickle blood contains tissue factor-positive microparticles derived from endothelial cells and monocytes. Blood 102 (7): 2678-2683. |
[11] | Combes V, Coltel N, Alibert M, Van Eck M, Raymond C, Juhan-Vague I, Grau GE, Chimini G (2005). ABCA1 gene deletion protects against cerebral malaria: potential pathogenic role of microparticles in neuropathology. Am J Pathol 166(1): 295-302. |
[12] | Allan D, Limbrick AR, Thomas P, Westerman MP (1981). Microvesicles from sickle erythrocytes and their relation to irreversible sickling. Br J Haematol 47: 383-390 |
[13] | Doeuvre L, Plawinski L, Toti F, Anglés-Cano E (2009). Cell-derived microparticles: a new challenge in neuroscience. Journal of Neurochemistry 110(2): 457-468. |
APA Style
Samuel Antwi-Baffour, Abena Nyarkoah Wiredu, Ransford Kyeremeh, Seidu Abdulai Mahmood. (2013). Plasma Membrane-Derived Vesicles in Sickle Cell Disease: A Possible Indicator of the Continuous Endothelial Stimulation and/or Injury to Blood Cells. American Journal of Biomedical and Life Sciences, 1(4), 99-102. https://doi.org/10.11648/j.ajbls.20130104.14
ACS Style
Samuel Antwi-Baffour; Abena Nyarkoah Wiredu; Ransford Kyeremeh; Seidu Abdulai Mahmood. Plasma Membrane-Derived Vesicles in Sickle Cell Disease: A Possible Indicator of the Continuous Endothelial Stimulation and/or Injury to Blood Cells. Am. J. Biomed. Life Sci. 2013, 1(4), 99-102. doi: 10.11648/j.ajbls.20130104.14
AMA Style
Samuel Antwi-Baffour, Abena Nyarkoah Wiredu, Ransford Kyeremeh, Seidu Abdulai Mahmood. Plasma Membrane-Derived Vesicles in Sickle Cell Disease: A Possible Indicator of the Continuous Endothelial Stimulation and/or Injury to Blood Cells. Am J Biomed Life Sci. 2013;1(4):99-102. doi: 10.11648/j.ajbls.20130104.14
@article{10.11648/j.ajbls.20130104.14, author = {Samuel Antwi-Baffour and Abena Nyarkoah Wiredu and Ransford Kyeremeh and Seidu Abdulai Mahmood}, title = {Plasma Membrane-Derived Vesicles in Sickle Cell Disease: A Possible Indicator of the Continuous Endothelial Stimulation and/or Injury to Blood Cells}, journal = {American Journal of Biomedical and Life Sciences}, volume = {1}, number = {4}, pages = {99-102}, doi = {10.11648/j.ajbls.20130104.14}, url = {https://doi.org/10.11648/j.ajbls.20130104.14}, eprint = {https://article.sciencepublishinggroup.com/pdf/10.11648.j.ajbls.20130104.14}, abstract = {Plasma membrane-derived vesicles (PMVs) are released into circulation in response to normal and stress/pathogenic conditions. They are of tremendous significance for the prediction, diagnosis, and observation of the therapeutic success of many diseases. Knowledge of their functional properties would contribute to a better understanding of the pathological mechanisms leading to various diseases in which their levels are raised. The objective of this study was to quantify and compare the levels of PMVs in sickle cell disease patients (Hb SS and Hb SC) with non-sickle cell (Hb AA) subjects. The comparison will help us research and understand the processes that lead to their constitutive release in sickle cell disease patients than in their normal counterparts. A total of one hundred and fifty (150) sickle cell disease patients (study group) and blood donors (control group) that consented to partake in the study were recruited. There were 82 males and 68 females. Fifty (50) each of Hb SS, Hb SC and Hb AA samples were obtained. Sodium metabisulphite (sickling) test, Haemoglobin electrophoresis and quantification of PMVs were carried out on all the samples. The sickle cell disease patients had elevated levels; SS (38.89 ± 0.73 × 104/ml; p= 0.01) and SC (32.62 ± 1.18 × 104/ml; p = 0.01) as against the control subjects (Hb AA) who had average PMVs of 11.28 ± 0.29 × 104/ml PFP (mean ± SEM). It was concluded that both SS and SC (study) samples showed an increased count of PMVs as compared to the AA (control) samples, suggesting persistent endothelial stimulation and/or injury of blood cells leading to continuous shedding of PMVs in sickle cell disease patients.}, year = {2013} }
TY - JOUR T1 - Plasma Membrane-Derived Vesicles in Sickle Cell Disease: A Possible Indicator of the Continuous Endothelial Stimulation and/or Injury to Blood Cells AU - Samuel Antwi-Baffour AU - Abena Nyarkoah Wiredu AU - Ransford Kyeremeh AU - Seidu Abdulai Mahmood Y1 - 2013/12/30 PY - 2013 N1 - https://doi.org/10.11648/j.ajbls.20130104.14 DO - 10.11648/j.ajbls.20130104.14 T2 - American Journal of Biomedical and Life Sciences JF - American Journal of Biomedical and Life Sciences JO - American Journal of Biomedical and Life Sciences SP - 99 EP - 102 PB - Science Publishing Group SN - 2330-880X UR - https://doi.org/10.11648/j.ajbls.20130104.14 AB - Plasma membrane-derived vesicles (PMVs) are released into circulation in response to normal and stress/pathogenic conditions. They are of tremendous significance for the prediction, diagnosis, and observation of the therapeutic success of many diseases. Knowledge of their functional properties would contribute to a better understanding of the pathological mechanisms leading to various diseases in which their levels are raised. The objective of this study was to quantify and compare the levels of PMVs in sickle cell disease patients (Hb SS and Hb SC) with non-sickle cell (Hb AA) subjects. The comparison will help us research and understand the processes that lead to their constitutive release in sickle cell disease patients than in their normal counterparts. A total of one hundred and fifty (150) sickle cell disease patients (study group) and blood donors (control group) that consented to partake in the study were recruited. There were 82 males and 68 females. Fifty (50) each of Hb SS, Hb SC and Hb AA samples were obtained. Sodium metabisulphite (sickling) test, Haemoglobin electrophoresis and quantification of PMVs were carried out on all the samples. The sickle cell disease patients had elevated levels; SS (38.89 ± 0.73 × 104/ml; p= 0.01) and SC (32.62 ± 1.18 × 104/ml; p = 0.01) as against the control subjects (Hb AA) who had average PMVs of 11.28 ± 0.29 × 104/ml PFP (mean ± SEM). It was concluded that both SS and SC (study) samples showed an increased count of PMVs as compared to the AA (control) samples, suggesting persistent endothelial stimulation and/or injury of blood cells leading to continuous shedding of PMVs in sickle cell disease patients. VL - 1 IS - 4 ER -